• 作者：Jian Wang^a ; ^b ; ^c ; ¹ ; Chenting Zhang^a ; ¹ ; Zili Zhang^a ; ¹ ; Zeguang Zheng^a ; ¹ ; Dejun Sun^b ; ¹ ; Quan Yang^a ; ¹ ; Cyrus Hadadi^d ; Defu Li^a ; Xiaoming Xu^a ; Mingmei Xiong^a ; Qipeng Zhou^a ; Meihua Guo^a ; Yingfeng Wang^a ; Chun Tang^a ; Guihua Xu^b ; Kai Yang^a ; Nanshan Zhong^a ; Wenju Lu^a ; ^{wlu92@yahoo.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：COPD ; BMPR2 ; rs6435156 ; Cigarette smoking ; hsa-miR-20a
• 刊名：EBioMedicine
• 出版年：2016
• 出版时间：March 2016
• 年：2016
• 卷：5
• 期：Complete
• 页码：167-174
• 全文大小：722 K

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The rs6435156 TT was associated with greater risk of COPD in smokers than in non-smokers.

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Cigarette smokers with rs6435156 TT were more susceptible to COPD than those with CC genotype.

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The T genotype of rs6435156 inhibited BMPR2 expression in PBMCs and lung epithelial cells.

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The rs6435156 T is the functional binding site for miR-20a.

COPD is characterized by abnormal inflammation and structural remodeling in the airway. Bone morphogenetic protein receptor type 2 (BMPR2) mediated signaling has been demonstrated to regulate pro-inflammatory responses in vasculature, and decreased expression of BMPR2 was found in COPD lungs; however the relationship of BMPR2 to COPD is unknown. We found that rs6435156 TT was the functional binding site for miR-20a in 3′UTR of BMPR2 and significantly increased risk of COPD in southern Chinese population; rs6435156C > T could modulate the susceptibility to COPD by interacting with cigarette smoking, which down-regulated BMPR2 expression dependent in hsa-miR-20a.